Charleston, SC, United States

Medical University of South Carolina
Charleston, SC, United States

The Medical University of South Carolina opened in Charleston, South Carolina in 1824 as a small private college for the training of physicians. It is one of the oldest continually operating schools of medicine in the United States and the oldest in the Deep South. The school's main building was designed by Charleston architect Albert W. Todd. The school has expanded into a state university with a medical center and six colleges for the education of health professionals, biomedical scientists and other health care personnel. It also operates as a center for research and has a public hospital. Wikipedia.

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University of Pittsburgh and Medical University of South Carolina | Date: 2016-10-13

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Flume P.A.,Medical University of South Carolina | VanDevanter D.R.,Case Western Reserve University
Advanced Drug Delivery Reviews | Year: 2015

The treatment of infection typically involves administration of antibiotics by a systemic route, such as intravenous or oral. However, pulmonary infections can also be approached by inhalation of antibiotics as the infection is more directly accessible via the airways, making inhalation delivery essentially topical administration. This approach offers deposition of high antimicrobial concentrations directly at the site of infection but with a potentially reduced systemic exposure. This review covers the evidence for aerosolized antibiotics for the treatment of a number of conditions such as cystic fibrosis (CF), where it has become the standard of care for chronic infection, as well as non-CF bronchiectasis, non-tuberculous mycobacteria, and ventilator-associated infection where such therapy does not have an approved indication but has been used with increasing frequency. © 2014 Elsevier B.V.

Eckert M.A.,Medical University of South Carolina
Frontiers in Neuroscience | Year: 2011

Processing speed, or the rate at which tasks can be performed, is a robust predictor of agerelated cognitive decline and an indicator of independence among older adults. This review examines evidence for neurobiological predictors of age-related changes in processing speed, which is guided in part by our source based morphometry findings that unique patterns of frontal and cerebellar gray matter predict age-related variation in processing speed. These results, together with the extant literature on morphological predictors of age-related changes in processing speed, suggest that specific neural systems undergo declines and as a result slow processing speed. Future studies of processing speed - dependent neural systems will be important for identifying the etiologies for processing speed change and the development of interventions that mitigate gradual age-related declines in cognitive functioning and enhance healthy cognitive aging. © 2011 Eckert.

Lopez M.F.,Medical University of South Carolina
Physiology and Behavior | Year: 2015

This study was designed to determine the impact of an enriched environment in a previously established stress model of isolation during early development that induces high alcohol (ethanol) self-administration. The study was conducted with male and female C57BL/6J mice housed in isolation or in groups that were either provided or withheld enrichment during adolescence. The impact of these housing conditions was assessed during adulthood by measuring weight gain, quantifying voluntary ethanol intake, measuring plasma corticosterone levels, and assessing anxiety-like behavior. Results showed that, regardless of sex, mice that were single-housed during adolescence showed a significant increase in voluntary ethanol intake, which was not observed in isolated mice that were provided with nesting material during adolescence (compared to group-housed non-enriched control group). Basal corticosterone was not affected by housing, enrichment conditions, or sex. Corticosterone levels did not relate to levels of voluntary ethanol intake. However, corticosterone levels were higher after three weeks of ethanol intake. Surprisingly, mice that were group-housed during adolescence showed higher levels of anxiety-like behavior in the light/dark test. Overall, these results indicate that housing conditions during a critical developmental period can significantly modulate voluntary ethanol intake later in life. © 2014.

Moorman D.E.,Medical University of South Carolina | Aston-Jones G.,Medical University of South Carolina
Journal of Neuroscience | Year: 2014

Adaptive execution and inhibition of behavior are guided by the activity of neuronal populations across multiple frontal cortical areas. The rodent medial prefrontal cortex has been well studied with respect to these behaviors, influencing behavioral execution/inhibition based on context. Other frontal regions, in particular the orbitofrontal cortex (OFC), are critical in directing behavior to obtain rewards, but the relationship between OFC neuronal activity and response execution or inhibition has been poorly characterized. In particular, little is known about OFC with respect to extinction learning, an important example of context-guided response inhibition. Here, we recorded the activity of OFC neurons while rats performed a discriminative-stimulus (DS)-driven sucrose-seeking task followed by multiple days ofextinction ofthe DS. OFC neuronal activity was maximally responsive (1) to reward-predicting stimuli(RS) thattriggered a lever press (i.e., lever-response initiation) and (2) during reward-well approach in pursuit of sucrose (i.e., well-response initiation). RS presentation that was not followed by a lever press or RS presentation during extinction produced weak activation, as did nonrewarded stimulus (NS) presentation regardless of response (press or withhold) or session (DS-sucrose or extinction). Activity related to nonrewarded well entry was minor, and activity was significantly inhibited during reward consumption. Finally, OFC neuronal activity switched selectivity to track rewarded behaviors when the RS/NS contingencies were reversed. Thus, rather than signaling variables related to extinction or response inhibition, activity in OFC was strongest at the initiation of multiple components of reward-seeking behavior, most prominently when valid reward-predicting cues drove these behaviors. © 2014 the authors.

Mahler S.V.,Medical University of South Carolina | Aston-Jones G.S.,Medical University of South Carolina
Journal of Neuroscience | Year: 2012

Ventral tegmental area (VTA) dopamine neurons are crucial for appetitive responses to Pavlovian cues, including cue-induced reinstatement of drug seeking. However, it is unknown which VTA inputs help activate these neurons, transducing stimuli into salient cues that drive drug-seeking behavior. Here we examined 56 VTA afferents from forebrain and midbrain that are Fos activated during cue-induced reinstatement. We injected the retrograde tracer cholera toxin β subunit (CTb) unilaterally into rostral or caudal VTA of male rats. All animals were trained to self-administer cocaine, then extinguished of this behavior. On a final test day, animals were exposed to response-contingent cocaine-associated cues, extinction conditions, a non-cocaine-predictive CS-, or a novel environment, and brains were processed to visualize CTb and Fos immunoreactivity to identify VTA afferents activated in relation to behaviors. VTA-projecting neurons in subregions of medial accumbens shell, ventral pallidum, elements of extended amygdala, and lateral septum (but not prefrontal cortex) were activated specifically during cue-induced cocaine seeking, and some of these were also activated proportionately to the degree of cocaine seeking. Surprisingly, though efferents from the lateral hypothalamic orexin field were also Fos activated during reinstatement, these were largely non-orexinergic. Also, VTA afferents from the rostromedial tegmental nucleus and lateral habenula were specifically activated during extinction and CS- tests, when cocaine was not expected. These findings point to a select set of subcortical nuclei which provide reinstatement-related inputs to VTA, translating conditioned stimuli into cocaine-seeking behavior. © 2012 the authors.

The question of whether cigarette smoking was associated with lung cancer was central to the expansion of epidemiology into the study of chronic diseases in the 1950s. The culmination of this era was the 1964 report of the Advisory Committee to the Surgeon General, a landmark document that included an objective synthesis of the evidence of the health consequences of smoking according to causal criteria. The report concluded that cigarette smoking was a cause of lung cancer in men and sufficient in scope that "remedial action" was warranted at the societal level. The 2014 Surgeon General's report commemorates the 50th anniversary of the 1964 report. The evidence on the health consequences of smoking has been updated many times in Surgeon General's reports since 1964. These have summarized our increasingly greater understanding of the broad spectrum of the deleterious health effects of exposure to tobacco smoke across most major organ systems. In turn, this evidence has been translated into tobacco control strategies implemented to protect the public's health. The Surgeon General report process is an enduring example of evidence-based public health in practice. Substantial progress has been made, but cigarette smoking remains one of the most pressing global health issues of our time. © The Author 2013.

Gooz M.,Medical University of South Carolina
Critical Reviews in Biochemistry and Molecular Biology | Year: 2010

This review focuses on the role of ADAM-17 in disease. Since its debut as the tumor necrosis factor converting enzyme (TACE), ADAM-17 has been reported to be an indispensible regulator of almost every cellular event from proliferation to migration. The central role of ADAM-17 in cell regulation is rooted in its diverse array of substrates: cytokines, growth factors, and their receptors as well as adhesion molecules are activated or inactivated by their cleavage with ADAM-17. It is therefore not surprising that ADAM-17 is implicated in numerous human diseases including cancer, heart disease, diabetes, rheumatoid arthritis, kidney fibrosis, Alzheimer's disease, and is a promising target for future treatments. The specific role of ADAM-17 in the pathophysiology of these diseases is very complex and depends on the cellular context. To exploit the therapeutic potential of ADAM-17, it is important to understand how its activity is regulated and how specific organs and cells can be targeted to inactivate or activate the enzyme. © 2010 Informa UK Ltd.

Henggeler S.W.,Medical University of South Carolina
Annual Review of Clinical Psychology | Year: 2011

The 35-year progression of multisystemic therapy (MST) from modest university-based efficacy studies to large-scale transport to community practice settings is described in this review. The success of early efficacy research led to effectiveness trials, and their success in decreasing rates of youth rearrest and incarceration led to multisite transportability trials and adaptations of the MST model for treating youth presenting other types of challenging clinical problems. To support the transport of MST programs to community settings, an intensive quality improvement system modeled after that used in clinical trials has been implemented in community-based MST programs for the past 15 years. With the association between therapist treatment fidelity and youth outcomes well established, transportability research has demonstrated the significant roles played by clinical supervisors, expert consultants, and provider organizations in supporting therapist adherence and youth outcomes. This body of work has been facilitated by federal and state initiatives to support evidence-based services. Copyright © 2011 by Annual Reviews. All rights reserved.

Liu B.,Medical University of South Carolina
Nature communications | Year: 2010

Cytosolic HSP90 requires multiple cochaperones in folding client proteins. However, the function of gp96 (HSP90b1, grp94), an HSP90 paralogue in the endoplasmic reticulum (ER), is believed to be independent of cochaperones. Here, we demonstrate that gp96 chaperones multiple Toll-like receptors (TLRs), but not TLR3, in a manner that is dependent on another ER luminal protein, CNPY3. gp96 directly interacts with CNPY3, and the complex dissociates in the presence of adenosine triphosphate (ATP). Genetic disruption of gp96-CNPY3 interaction completely abolishes their TLR chaperone function. Moreover, we demonstrate that TLR9 forms a multimolecular complex with gp96 and CNPY3, and the binding of TLR9 to either molecule requires the presence of the other. We suggest that CNPY3 interacts with the ATP-sensitive conformation of gp96 to promote substrate loading. Our study has thus established CNPY3 as a TLR-specific cochaperone for gp96.

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